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Analysis of Ca2+-triggered Ras GTPase-activating protein function

ReferenceBBS/E/B/0000C197
Principal Investigator / Supervisor Dr Simon Cook
Co-Investigators /
Co-Supervisors
Professor Len Stephens
Institution Babraham Institute
DepartmentBabraham Institute Department
Funding typeResearch
Value (£) 649,357
StatusCompleted
TypeInstitute Project
Start date 27/01/2005
End date 26/01/2008
Duration36 months

Abstract

Cells need to sense changes in their environment in order to survive and grow. An important mechanism involves the communication of a signal from the cell surface into the cell. Ras proteins are located on cell membranes and serve a critical role in receiving and decoding signals from cell surface receptors. They are binary switches, responding to receptor stimulation by switching to an active conformation that signals to effector pathways to regulate gene expression. Ras genes are mutated in human cancers and have been shown to induce changes associated with the tumorigenic state; therefore they are described as proto-oncogenes. They are mutated to an active form in up to 30% of human cancers. Understanding how the Ras switch is activated and inhibited is therefore critical for human health. We recently discovered novel inhibitors of the Ras switch called CAPRI and RASAL that promote the Ras `off state¿ in a Ca2+-dependent manner. These are Ras GTPase-activating proteins (GAPs). We wish to discover more about the intrinsic function of Ca2+-regulated GAPs by gene disruption in the mouse. This will lead to a greater understanding of the mechanisms by which Ras is regulated during receptor-stimulated Ca2+ signals.

Summary

unavailable
Committee Closed Committee - Biochemistry & Cell Biology (BCB)
Research TopicsX – not assigned to a current Research Topic
Research PriorityX – Research Priority information not available
Research Initiative X - not in an Initiative
Funding SchemeX – not Funded via a specific Funding Scheme
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